scholarly journals Antihypertensive Effects of Gynura divaricata (L.) DC in Rats with Renovascular Hypertension

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3321 ◽  
Author(s):  
Mi Hyeon Hong ◽  
Xian Jun Jin ◽  
Jung Joo Yoon ◽  
Yun Jung Lee ◽  
Hyun Cheol Oh ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Traditional Medicine ◽  
Kidney Function ◽  
Natriuretic Peptide ◽  
High Blood Pressure ◽  
Periodic Acid ◽  
Urine Volume ◽  
Heart Weight ◽  
Excretory Function ◽  
Renal Excretory Function

Gynura divaricata (L.) DC (Compositae) (GD) could be found in various parts of Asia. It has been used as a traditional medicine to treat diabetes, high blood pressure, and other diseases, but its effects have not yet been scientifically confirmed. Therefore, we aimed at determining whether GD could affect renal function regulation, blood pressure, and the renin-angiotensin-aldosterone system (RAAS). Cardio-renal syndrome (CRS) is a disease caused by the interaction between the kidney and the cardiovascular system, where the acute or chronic dysfunction in one organ might induce acute or chronic dysfunction of the other. This study investigated whether GD could improve cardio-renal mutual in CRS type 4 model animals, two-kidney one-clip (2K1C) renal hypertensive rats. The experiments were performed on the following six experimental groups: control rats (CONT); 2K1C rats (negative control); OMT (Olmetec, 10 mg/kg/day)-treated 2K1C rats (positive control); and 2K1C rats treated with GD extracts in three different doses (50, 100, and 200 mg/kg/day) for three weeks by oral intake. Each group consisted of 10 rats. We measured the systolic blood pressure weekly using the tail-cuff method. Urine was also individually collected from the metabolic cage to investigate the effect of GD on the kidney function, monitoring urine volume, electrolyte, osmotic pressure, and creatinine levels from the collected urine. We observed that kidney weight and urine volume, which would both display typically increased values in non-treated 2K1C animals, significantly decreased following the GD treatment (###p < 0.001 vs. 2K1C). Osmolality and electrolytes were measured in the urine to determine how renal excretory function, which is reduced in 2K1C rats, could be affected. We found that the GD treatment improved renal excretory function. Moreover, using periodic acid-Schiff staining, we confirmed that the GD treatment significantly reduced fibrosis, which is typically increased in 2K1C rats. Thus, we confirmed that the GD treatment improved kidney function in 2K1C rats. Meanwhile, we conducted blood pressure and vascular relaxation studies to determine if the GD treatment could improve cardiovascular function in 2K1C rats. The heart weight percentages of the left atrium and ventricle were significantly lower in GD-treated 2K1C rats than in non-treated 2K1C rats. These results showed that GD treatment reduced cardiac hypertrophy in 2K1C rats. Furthermore, the acetylcholine-, sodium nitroprusside-, and atrial natriuretic peptide-mediated reduction of vasodilation in 2K1C rat aortic rings was also ameliorated by GD treatment (GD 200 mg/kg/day; p < 0.01, p < 0.05, and p < 0.05 vs. 2K1C for vasodilation percentage in case of each compound). The mRNA expression in the 2K1C rat heart tissue showed that the GD treatment reduced brain-type natriuretic peptide and troponin T levels (p < 0.001 and p < 0.001 vs. 2K1C). In conclusion, this study showed that GD improved the cardiovascular and renal dysfunction observed in an innovative hypertension model, highlighting the potential of GD as a therapeutic agent for hypertension. These findings indicate that GD shows beneficial effects against high blood pressure by modulating the RAAS in the cardio-renal syndrome. Thus, it should be considered an effective traditional medicine in hypertension treatment.

Association of B-Type Natriuretic Peptide Level with Residual Kidney Function in Incident Peritoneal Dialysis Patients

2019 ◽  
Vol 39 (2) ◽  
pp. 147-154 ◽  
Author(s):  
Yasuhiro Kawai ◽  
Shigeru Tanaka ◽  
Hisako Yoshida ◽  
Masatoshi Hara ◽  
Hiroaki Tsujikawa ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Kidney Function ◽  
Natriuretic Peptide ◽  
Subgroup Analysis ◽  
Proportional Hazards Model ◽  
Urine Volume ◽  
Cox Proportional Hazards Model ◽  
University Hospital ◽  
Residual Kidney Function ◽  
Increased Risk

Background Residual kidney function (RKF) is an important factor influencing both technique and patient survival in peritoneal dialysis (PD) patients. B-type natriuretic peptide (BNP) is considered a marker of cardio-renal syndrome. The relationship between BNP and RKF in PD patients remains unclear. Methods We conducted a prospective study of 89 patients who had started and continued PD for 6 months or more in Kyushu University Hospital between June 2006 and September 2015. Participants were divided into low BNP (≤ 102.1 ng/L) and high BNP (> 102.1 ng/L) groups according to median plasma BNP level at PD initiation. The primary outcome was RKF loss, defined as 24-hour urine volume less than 100 mL. We estimated the association between BNP and RKF loss using a Kaplan-Meier method and Cox proportional hazards model and compared the rate of RKF decline between the 2 groups. To evaluate the consistency of the association, we performed subgroup analysis stratified by baseline characteristics. Results During the median follow-up of 30 months, 30 patients lost RKF. Participants in the high BNP group had a 5.87-fold increased risk for RKF loss compared with the low BNP group after adjustment for clinical and cardiac parameters. A high plasma BNP level was more clearly associated with RKF loss in younger participants compared with older participants in subgroup analysis. Conclusions B-type natriuretic peptide may be a useful risk marker for RKF loss in PD patients. The clinical importance of plasma BNP level as a marker of RKF loss might be affected by age.

Natriuretic peptide analogues with distinct vasodilatory or renal activity: integrated effects in health and experimental heart failure

2020 ◽  
Author(s):  
Miriam T Rademaker ◽  
Nicola J A Scott ◽  
Cho Yeow Koh ◽  
R Manjunatha Kini ◽  
A Mark Richards
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Natriuretic Peptide ◽  
Acute Decompensated Heart Failure ◽  
Unmet Need ◽  
Urine Volume ◽  
Plasma Renin ◽  
Decompensated Heart Failure ◽  
Guanosine Monophosphate ◽  
High Dose

Abstract Aims Management of acute decompensated heart failure (ADHF) requires disparate treatments depending on the state of systemic/peripheral perfusion and the presence/absence of expanded body–fluid volumes. There is an unmet need for therapeutics that differentially treat each aspect. Atrial natriuretic peptide (ANP) plays an important role in blood pressure and volume regulation. We investigate for the first time the integrated haemodynamic, endocrine and renal effects of human ANP analogues, modified for exclusive vasodilatory (ANP-DRD) or diuretic (ANP-DGD) activities, in normal health and experimental ADHF. Methods and results We compared the effects of incremental infusions of ANP analogues ANP-DRD and ANP-DGD with native ANP, in normal (n = 8) and ADHF (n = 8) sheep. ANP-DRD administration increased plasma cyclic guanosine monophosphate (cGMP) in association with dose-dependent reductions in arterial pressure in normal and heart failure (HF) sheep similarly to ANP responses. In contrast to ANP, which in HF produced a diuresis/natriuresis, this analogue was without significant renal effect. Conversely, ANP-DGD induced marked stepwise increases in urinary cGMP, urine volume, and sodium excretion in HF comparable to ANP, but without accompanying vasodilatory effects. All peptides increased packed cell volume relative to control in both states, and in HF, decreased left atrial pressure. In response to ANP-DRD-induced blood pressure reductions, plasma renin activity rose compared to control only during the high dose in normals, and not at all in HF—suggesting relative renin inhibition, with no increase in aldosterone in either state, whereas renin and aldosterone were both significantly reduced by ANP-DGD in HF. Conclusion These ANP analogues exhibit distinct vasodilatory (ANP-DRD) and diuretic/natriuretic (ANP-DGD) activities, and therefore have the potential to provide precision therapy for ADHF patients with differing pathophysiological derangement of pressure–volume homeostasis.

scholarly journals STUDIES ON EXPERIMENTAL HYPERTENSION

1941 ◽  
Vol 73 (3) ◽  
pp. 439-451 ◽  
Author(s):  
Harry Goldblatt ◽  
Harry Weinstein ◽  
Joseph R. Kahn
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Arterial Occlusion ◽  
Experimental Hypertension ◽  
Excretory Function ◽  
Main Renal Artery ◽  
Significant Impairment ◽  
Temporary Occlusion ◽  
Renal Origin ◽  
Renal Excretory Function

By means of a silver chain attached to a silver ring around the main renal artery, intermittent renal arterial occlusion, up to 30 minutes daily, was practiced for as long as 5 months in unilaterally nephrectomized dogs. This did not result in the development of persistently elevated blood pressure. Persistent moderate constriction of the renal artery of such animals by a silver clamp, after intermittent temporary occlusion had failed to affect the blood pressure, produced the usual rise of blood pressure, without accompanying significant impairment of renal excretory function. When the renal artery accidentally became persistently constricted to a great degree, or actually occluded, or if occlusion was deliberately produced by continuous pulling of the chain, hypertension and renal insufficiency (the malignant phase) quickly developed. The results do not lend support to the view that brief daily periods of renal ischemia from intrarenal vasospasm, or from any other cause, can produce persistent hypertension of renal origin.

scholarly journals Complications of Polycystic Kidney Disease and Relation With Disease Progression: An Observational Retrospective Study

2020 ◽  
Author(s):  
Mònica Pérez-Mir ◽  
Laura Carreras-Planella ◽  
Francesc Borràs ◽  
Josep Bonet ◽  
Maribel Troya
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Retrospective Study ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Kidney Function ◽  
High Blood Pressure ◽  
Inherited Disease ◽  
Polycystic Kidney ◽  
Renal Complication

Abstract Background: Autosomal dominant polycystic kidney disease (ADPKD) is a renal inherited disease characterized by the growth of bilateral renal cysts that lead to deterioration in renal function and end-stage renal disease (ESRD). These patients frequently present complications like urinary tract infection, acute pyelonephritis, acute or chronic pain, renal lithiasis or high blood pressure (HBP). The aim of this study is to compare the renal evolution in ADPKD patients with renal complications and/or HBP compared to those without complications nor HBP.Methods: Observational retrospective study of 29 ADPKD patients with normal renal function and <70 years followed up in our center. Clinical and analytical information of 2010, 2015 and 2017 were determined.Results: 29 patients were enrolled with a median age of 41 years [34-54], eighteen women (62,1%) and eleven men. Median of estimation of glomerular function rate (eGFR) was 85.8ml/min [70.7-115.6] in 2010, 76.0 ml/min [57.0-99.9] in 2015 and 63.1ml/min [45.0-95.8] in 2017. Eight patients (27.6%) have never had kidney complication nor HBP. Nine patients (31.0%) have normal blood pressure, 6 others (20.7%) have well controlled high blood pressure (HBP) and 14 (48.3%) have badly controlled HBP. When patients were divided between those who have never presented a complication (C-) and those who present renal complication and/or HBP (C+), the first group presented better kidney function. When patients were segregated into those who have never presented complication or well-controlled HBP (CHBP-) and those with renal complication and/or badly-controlled HBP (CHBP+) no differences were found at the initial eGFR, but a faster worsening of kidney function in CHBP+ group.Conclusions: In ADPKD patients, the decrease in eGFR is significantly important in individuals showing complications (including HBP) compared to those who did not present complications. Individuals with complications and badly-controlled HBP show even greater differences in kidney function decrease compared with patients without complications or well controlled HBP.

DOES HIGH BLOOD PRESSURE INFLUENCE PLASMA LEVELS OF B-TYPE NATRIURETIC PEPTIDE?

2004 ◽  
Vol 22 (Suppl. 1) ◽  
pp. S152
Author(s):  
Tomas Janota ◽  
P. Jakubik ◽  
J. Hradec ◽  
H. Benakova ◽  
D. Wichterle ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Natriuretic Peptide ◽  
High Blood Pressure ◽  
Plasma Levels

scholarly journals Cardioprotective Effects of the Novel Compound Vastiras in a Preclinical Model of End-Organ Damage

Hypertension ◽  
2020 ◽  
Vol 75 (5) ◽  
pp. 1195-1204
Author(s):  
Raffaele Altara ◽  
Gustavo J.J. da Silva ◽  
Michael Frisk ◽  
Francesco Spelta ◽  
Fouad A. Zouein ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Renal Damage ◽  
Weight Ratio ◽  
Hypertensive Heart Disease ◽  
Heart Weight ◽  
Preclinical Model ◽  
Continuous Administration ◽  
Positive Effects

Cardiac hypertrophy and renal damage associated with hypertension are independent predictors of morbidity and mortality. In a model of hypertensive heart disease and renal damage, we tested the actions of continuous administration of Vastiras, a novel compound derived from the linear fragment of ANP (atrial natriuretic peptide), namely pro-ANP 31–67 , on blood pressure and associated renal and cardiac function and remodeling. Of note, this peptide, unlike the ring structured forms, does not bind to the classic natriuretic peptide receptors. Dahl/Salt–Sensitive rats fed a 4% NaCl diet for 6 weeks developed hypertension, cardiac hypertrophy, and renal damage. Four weeks of treatment with 50 to 100 ng/kg per day of Vastiras exhibited positive effects on renal function, independent of blood pressure regulation. Treated rats had increased urine excretion, natriuresis, and enhanced glomerular filtration rate. Importantly, these favorable renal effects were accompanied by improved cardiac structure and function, including attenuated cardiac hypertrophy, as indicated by decreased heart weight to body weight ratio, relative wall thickness, and left atrial diameter, as well as reduced fibrosis and normalized ratio of the diastolic mitral inflow E wave to A wave. A renal subtherapeutic dose of Vastiras (25 ng/kg per day) induced similar protective effects on the heart. At the cellular level, cardiomyocyte size and t-tubule density were preserved in Vastiras-treated compared with untreated animals. In conclusion, these data demonstrate the cardiorenal protective actions of chronic supplementation of a first-in-class compound, Vastiras, in a preclinical model of maladaptive cardiac hypertrophy and renal damage induced by hypertension.

scholarly journals Kidney function in mice lacking aldosterone

2006 ◽  
Vol 290 (1) ◽  
pp. F61-F69 ◽  
Author(s):  
Natalia Makhanova ◽  
Gene Lee ◽  
Nobuyuki Takahashi ◽  
Maria L. Sequeira Lopez ◽  
R. Ariel Gomez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Function ◽  
Plasma Concentrations ◽  
Urine Volume ◽  
Weight Ratio ◽  
Urine Osmolality ◽  
Dietary Salt ◽  
Water Metabolism ◽  
Low Blood Pressure ◽  
Cox 2

To explore the effects of decreased amounts or absence of aldosterone, we have disrupted the gene coding for aldosterone synthase (AS) in mice and investigated blood pressure and kidney function in AS+/+, AS+/−, and AS−/− mice. AS+/− mice have normal blood pressures and show no abnormalities in electrolytes or kidney gene expression, but they have significantly higher than normal urine volume and lower urine osmolality. In contrast, the AS−/− mice have low blood pressure, abnormal electrolyte homeostasis (increased plasma concentrations of K+, Ca2+, and Mg2+ and decreased concentrations of HCO3− and Cl− but no difference in the plasma Na+ level), and disturbances in water metabolism (higher urine output, decreased urine osmolality, and impaired urine concentrating and diluting ability). Absence of aldosterone in the AS−/− mice induced several compensatory changes: an increased food intake-to-body weight ratio, an elevated plasma concentration of glucocorticoids, and strong activation of the renin-angiotensin system. Parallel with the markedly increased synthesis and release of renin, the AS−/− mice showed increased expression of cyclooxygenase-2 (COX-2) in macula densa. On salt supplementation, plasma electrolyte concentrations and kidney renin and COX-2 levels became similar to those of wild-type mice, but the lower blood pressure of the AS−/− mice was not corrected. Thus absence of aldosterone in AS−/− mice results in impairment of Na+ reabsorption in the distal nephron, decreased blood pressure, and strong renin-angiontensin system activation. Our data show the substantial correction of these abnormalities, except the low blood pressure, by high dietary salt does not depend on aldosterone.

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